Note: Javascript is disabled or is not supported by your browser. For this reason, some items on this page will be unavailable. For more information about this message, please visit this page: About CDC.gov.

Persons whose skin or clothing is contaminated with liquid or powdered parathion can cause secondary contamination by direct contact.

Parathion is an organophosphate pesticide. At room temperature, it is a combustible pale yellow to dark brown liquid that may be difficult to ignite. In commercial products, parathion is usually dissolved in hydrocarbon solvents such as toluene or xylene, which are flammable. Parathion has a garlic-like odor, which does not provide adequate warning of hazardous concentrations.

Because parathion has a low vapor pressure, significant inhalation is unlikely at ordinary temperatures. However, the hydrocarbon solvents in commercial preparations can be inhaled. Parathion is rapidly absorbed by ingestion and through intact skin and the eyes, resulting in acute systemic toxicity.

General Information

Description

At room temperature, parathion is a yellow-to-brown liquid with an odor of garlic. It is often dissolved in a hydrocarbon solvent before use. Parathion itself is not volatile. It is almost insoluble in water, slightly soluble in petroleum oils, and miscible with many organic solvents.

Routes of Exposure

Inhalation

Toxic inhalation of parathion vapor is unlikely at ordinary temperatures because of its low volatility, but toxic effects can occur after inhalation of parathion sprays or dusts. The hydrocarbon solvents (most commonly toluene and xylene) used to dissolve parathion are more volatile than parathion itself, and toxicity can result from inhalation of solvent vapor as well. The odor threshold of parathion is five times the OSHA PEL (0.1 mg/m³) and does not provide adequate warning of hazardous concentrations.

Children exposed to the same levels of
parathion as adults may receive a larger dose because they have greater lung surface area:body weight ratios and increased minute volumes:weight ratios.

Skin/Eye Contact

Parathion is not irritating to the skin
or eyes, but is rapidly absorbed through intact skin and eyes,
contributing to systemic toxicity.

Children are more vulnerable to toxicants
absorbed through the skin because of their relatively larger
surface area:body weight ratio.

Ingestion

Acute toxic effects, including rapidly
fatal systemic poisoning, can result from ingestion of parathion.

Sources/Uses

Parathion is prepared by the reaction
of diethyl phosphorothionchloridate with sodium p-nitrophenate.
It is widely used as an agricultural insecticide. It has been
used extensively by U.S. farmers on major crops such as wheat,
fruit, vegetables, nuts, citrus fruits, alfalfa, corn, soybeans,
and other field crops.

Incompatibilities

Health Effects

Systemic toxicity due to parathion can result from all
routes of exposure. Symptoms include abdominal cramps, vomiting,
diarrhea, pinpoint pupils and blurred vision, excessive
sweating, salivation and lacrimation, wheezing, excessive
tracheobronchial secretions, agitation, seizures, bradycardia
or tachycardia, muscle twitching and weakness, and urinary
bladder and fecal incontinence. Seizures are much more common
in children than in adults.

Commercial parathion products often contain hydrocarbon
solvents, such as xylene or toluene, which themselves can
cause toxicity.

Toxicity of parathion depends on metabolic activation;
thus, symptoms may be delayed for 6 to 24 hours after exposure.

Acute Exposure

Parathion, like all organophosphate pesticides,
inhibits acetylcholinesterase and alters cholinergic synaptic
transmission at neuroeffector junctions (muscarinic effects),
at skeletal myoneural junctions and autonomic ganglia (nicotinic
effects), and in the CNS. Inhibition occurs when a metabolite
of parathion binds to acetylcholinesterase; thus, symptoms
may be delayed after exposure. Signs and symptoms of poisoning
vary according to age, dose, and concentration.

Peripheral Neurologic

Peripheral neurologic effects include
muscle twitching and weakness due to inhibition of acetylcholinesterase
at neuromuscular junctions.

Respiratory

Respiratory failure is the most common
cause of death due to parathion poisoning. Narrowing of the
bronchi and markedly increased bronchial secretions can occur.
Respiratory failure results from respiratory depression coupled
with paralysis of the respiratory muscles and progressive
airway obstruction from bronchorrhea. In addition, pulmonary
aspiration of the hydrocarbon solvents found in many commercial
preparations can cause inflammation of the lungs.

Children may be more vulnerable because
of relatively increased minute ventilation per kg and failure
to evacuate as area promptly when exposed.

Cardiovascular

Most exposure victims experience bradycardia,
but pulse rate may be increased initially and tachycardia
is more common in very severe poisoning. Irregular heartbeat
may occur.

Gastrointestinal

Nausea, vomiting, abdominal cramps, diarrhea,
and fecal incontinence are common manifestations, regardless
of the exposure route. These are generally the earliest symptoms
to occur.

Metabolic

Profuse sweating is likely to occur and
may lead to profound dehydration. This is somewhat less common
in children.

Dermal

Parathion is not generally irritating,
but is readily absorbed through the skin. Skin contact can
result in systemic poisoning.

Because of their relatively larger surface
area:body weight ratio, children are more vulnerable to toxicants
absorbed through the skin.

Ocular

Systemic poisoning typically causes pinpoint
pupils and spasm of the muscle of visual accommodation (i.e.,
ciliary muscle) leading to blurred vision and aching pain
in the eye. However, organophosphate poisoning may still be
present without pinpoint pupils, and dilation of the pupils
may even be noted occasionally. Eye irritation, if it occurs,
is most likely caused by the hydrocarbon solvents used in
commercial pesticide preparations.

Potential Sequelae

Complete recovery generally occurs within
10 days unless severe lack of oxygen has caused residual brain
damage. CNS effects such as confusion, fatigue, irritability,
nervousness, and impairment of memory can occasionally last
for several weeks. Six to twenty-one days after acute exposure
to some organophosphate compounds, onset of nerve disorders
of mixed sensory-motor type may occur; peripheral nerve recovery
may never be complete. It is uncertain if parathion produces
this delayed polyneuropathy.

Chronic Exposure

Persistent weakness and impaired memory
have been reported to occur from low-level exposures to organophosphates
in the absence of acute cholinergic effects.

Carcinogenicity

The International Agency for Research
on Cancer has determined that parathion is not classifiable
as to its carcinogenicity to humans. However, EPA lists parathion
as a possible human carcinogen.

Reproductive and Developmental Effects

Studies have been reported in which parathion
was embryo-toxic and fetotoxic in rodents. There are no studies
addressing reproductive or developmental effects in humans
exposed to parathion. Parathion is not included in Reproductive
and Developmental Toxicants, a 1991 report published by
the U.S. General Accounting Office (GAO) that lists 30 other
chemicals of concern because of widely acknowledged reproductive
and developmental consequences.

Prehospital Management

Parathion is highly contaminating. Victims whose skin
or clothing is contaminated with liquid or powdered parathion
can secondarily contaminate response personnel by direct
contact or evaporation of solvent vapor. Clothing and leather
goods (e.g., belts or shoes) cannot be reliably decontaminated;
they should be incinerated.

Commercial parathion products often contain hydrocarbon
solvents, such as xylene or toluene, which themselves can
cause toxicity. Treatment for breathing the solvent is fresh
air.

Treatment for parathion poisoning consists of thorough
decontamination, cardiorespiratory support, and administration
of the antidotes atropine and pralidoxime. Antidotes should
be administered as prevention even if the diagnosis is in
doubt.

Hot Zone

Rescuers should be trained and appropriately
attired before entering the Hot Zone. If the proper equipment
is not available, or if rescuers have not been trained in
its use, assistance should be obtained from a local or regional
HAZMAT team or other properly equipped response organization.

Rescuer Protection

Parathion is a highly toxic systemic
poison that is absorbed well by all routes of exposure.

Skin Protection: Chemical-protective
clothing is recommended because parathion is rapidly absorbed
through the skin and may cause systemic poisoning.

ABC Reminders

Quickly access for a patent airway, ensure
adequate respiration and pulse. If trauma is suspected, maintain
cervical immobilization manually and apply a cervical collar
and a backboard when feasible.

Victim Removal

If victims can walk, lead them out of
the Hot Zone to the Decontamination Zone. Victims who are
unable to walk may be removed on backboards or gurneys; if
these are not available, carefully carry or drag victims to
safety.

Consider appropriate management of chemically-contaminated
children, such as measures to reduce separation anxiety if
a child is separated from a parent or other adult.

Decontamination Zone

All victims suspected of parathion ingestion,
or substantial exposure to aerosolized parathion, or who have
skin or eye exposure to liquid or powdered parathion require
thorough decontamination as described below.

Rescuer Protection

If exposure levels are determined to
be safe, decontamination may be conducted by personnel wearing
a lower level of protection than that worn in the Hot Zone
(described above).

ABC Reminders

Quickly access for a patent airway, ensure
adequate respiration and pulse. Stabilize the cervical spine
with a collar and a backboard if trauma is suspected. Administer
supplemental oxygen as required. Assist ventilation with a
bag-valve-mask device if necessary.

Basic Decontamination

Rapid and thorough decontamination
is critical, but must proceed concurrently with supportive
and antidotal measures.

Victims who are able may assist with
their own decontamination. Quickly remove and double-bag contaminated
clothing and personal belongings. Clothing (especially leather
items) is extremely difficult to decontaminate; in most cases,
contaminated clothing should be incinerated as directed by
hazardous materials experts.

Victims should be washed repeatedly with
copious amounts of soap and water. Rescuers should wear rubber
gloves as vinyl gloves provide no protection against skin
absorption. It is important to observe the patient closely
for sudden appearance of symptoms. It is important to thoroughly
clean hair, fingernails, and skin folds. Use caution to avoid
hypothermia when decontaminating children or the elderly.
Use blankets or warmers when appropriate.

Irrigate exposed or irritated eyes with
plain water or saline for 15 minutes. Remove contact lenses
if easily removable without additional trauma to the eye.
If a corrosive material is suspected or if pain or injury
is evident, continue irrigation while transferring the victim
to the Support Zone.

In cases of ingestion, do not induce
emesis. If the victim is alert and asymptomatic, administer
a slurry of activated charcoal (at 1 gm/kg, usual adult dose
60-90 g, child dose 25-50 g). A soda can and straw may be
of assistance when offering charcoal to a child.

Consider appropriate management of chemically
contaminated children at the exposure site. Provide reassurance
to the child during decontamination, especially if separation
from a parent occurs.

Transfer to Support Zone

As soon as basic decontamination is complete,
move the victim to the Support Zone.

Support Zone

Be certain that victims have been decontaminated
properly (see Decontamination Zone above). Victims
who have undergone decontamination or have been exposed only
to vapor generally pose no serious risks of secondary contamination
to rescuers. However, the Support Zone team should wear disposable
aprons or gowns and rubber gloves for protection.

ABC Reminders

Quickly access for a patent airway. If
trauma is suspected, maintain cervical immobilization manually
and apply a cervical collar and a backboard when feasible.
Ensure adequate respiration and pulse. Administer supplemental
oxygen as required and establish intravenous access if necessary.
Place on a cardiac monitor. Airway suctioning may be required
for excessive bronchial secretions.

Additional Decontamination

Continue irrigating exposed skin and
eyes, as appropriate.

In cases of ingestion, do not induce
emesis. If the victim is alert and asymptomatic, administer
a slurry of activated charcoal if it has not already been
given (at 1 gm/kg, usual adult dose 60-90 g, child dose 25-50
g). A soda can and straw may be of assistance when offering
charcoal to a child.

Advanced Treatment

In cases of respiratory compromise, coma,
or to facilitate removal of excessive pulmonary secretions
secure airway and respiration via endotracheal intubation.
If not possible, perform cricothyroidotomy if equipped and
trained to do so.

When possible, atropine (see Antidotes,
below) should be given under medical supervision to all symptomatic
patients who have known or strongly suspected parathion poisoning.

Patients who are comatose, hypotensive,
or having seizures or cardiac arrhythmias should be treated
according to advanced life support (ALS) protocols.

Antidotes

Two antidotes are administered to treat
organophosphate poisoning. Atropine is a competitive antagonist
of acetylcholine at muscarinic receptors and is used to control
the excessive bronchial secretions which are often responsible
for death. Pralidoxime relieves both the nicotinic and muscarine
effects of organophosphate poisoning by regenerating acetylcholinesterase
and can reduce both the bronchial secretions and the muscle
weakness associated with poisoning.

The initial intravenous dose of atropine
in adults should be determined by the severity of symptoms:
An initial adult dose of 1.0 to 2.0 mg or pediatric dose of
0.01 mg/kg (minimum 0.01 mg) should be administered intravenously.
If intravenous access cannot be established, atropine may
also be given subcutaneously or via endotracheal tube. Doses
should be repeated every 15 minutes until excessive secretions
and sweating have been controlled. Once bronchial secretion
has been controlled, atropine administration should be repeated
whenever the secretions begin to recur. In seriously poisoned
patients, very large doses may be required. Alterations of
pulse rate and pupillary size should not be used as indicators
of treatment adequacy.

Pralidoxime should be administered as
early in poisoning as possible as its efficacy may diminish
when given more than 24 to 36 hours after exposure. Doses
are as follows: adult 1.0 g; pediatric 25 to 50 mg/kg. The
drug should be administered intravenously over 30 to 60 minutes,
but in a life-threatening situation, one-half of the total
dose can be given per minute for a total administration time
of 2 minutes. Treatment should begin to take effect within
40 minutes with a reduction in symptoms and the amount of
atropine necessary to control bronchial secretion. The initial
dose can be repeated in 1 hour and then every 8 to 12 hours
until the patient is clinically well and no longer requires
atropine.

Transport to Medical Facility

Only decontaminated patients or patients
not requiring decontamination should be transported to a medical
facility. "Body bags" are not recommended.

Report to the base station and the receiving
medical facility the condition of the patient, treatment given,
and estimated time of arrival at the medical facility. Severely
ill patients should be taken to a medical facility immediately.

If parathion has been ingested, prepare
the ambulance in case the victim vomits toxic material. Have
ready several towels and open plastic bags to quickly clean
up and isolate vomitus.

Multi-Casualty Triage

Consult with the base station physician
or the regional poison control center for advice regarding
triage of multiple victims.

Patients with evidence of significant
exposure, such as nausea or excessive sweating, and all persons
who have ingested parathion should be transported to a medical
facility for evaluation. Others may be discharged at the scene
after their names, addresses, and telephone numbers are recorded.
It is very important to ensure that individuals have been
completely decontaminated before discharge; otherwise life-threatening
symptoms may occur in the absence of assistance. Those discharged
should be advised to seek medical care promptly if symptoms
develop (see Patient Information Sheet below).

Emergency Department Management

Parathion is highly contaminating. Patients whose skin
or clothing is contaminated with liquid or powdered parathion
can secondarily contaminate hospital personnel by direct
contact or off-gassing of solvent vapor from clothing, skin,
or vomitus. Clothing and leather goods (e.g., belts or shoes)
cannot be reliably decontaminated; they should be incinerated.

Commercial parathion products often contain hydrocarbon
solvents such as xylene or toluene, which themselves can
cause toxicity.

Treatment consists of thorough decontamination, cardiorespiratory
support, and administration of the antidotes atropine and
pralidoxime. Antidotes should be administered as prevention
even if the diagnosis is in doubt.

Decontamination Area

Unless decontaminated previously, all
patients suspected of skin or eye contact with liquid or powdered
parathion require decontamination immediately. If a solvent
such as xylene or toluene is involved, decontamination should
take place outdoors or with proper ventilation.

Health care personnel should don butyl
rubber aprons and butyl rubber gloves. If butyl rubber items
are not available, limited protection will be provided by
two layers of latex gloves and a waterproof apron or chemical-resistant
jumpsuit. Wash hands frequently during decontamination and
promptly dispose of latex gloves. Personnel who come in contact
with parathion secondarily should undergo decontamination.

Be aware that use of protective equipment
by the provider may cause fear in children, resulting in decreased
compliance with further management efforts.

Because of their relatively larger surface
area:body weight ratio, children are more vulnerable to toxicants
absorbed through the skin. Also emergency room personnel should
examine children's mouths because of the frequency of hand-to-mouth
activity among children.

ABC Reminders

Evaluate and support airway, breathing,
and circulation. In cases of respiratory compromise, coma,
or to facilitate tracheal suctioning, secure airway and respiration
via endotracheal intubation. If not possible, surgically create
an airway. Suctioning may be required for excessive bronchial
secretions.

Patients who are comatose, hypotensive,
or have seizures or ventricular arrhythmias should be treated
in the conventional manner.

Basic Decontamination

Patients who are able may assist with
their own decontamination. Remove and double-bag contaminated
clothing and personal belongings. Dispose of contaminated
clothing and leather goods (e.g., belts, wallets, and shoes);
they should be incinerated as directed by hazardous materials
experts.

Victims should be washed repeatedly with
copious amounts of soap and water. Rescuers should wear rubber
gloves as vinyl gloves provide no protection against skin
absorption. It is important to observe the patient closely
for sudden appearance of symptoms. It is important to thoroughly
clean hair, fingernails, and skin folds.Use caution to avoid
hypothermia when decontaminating children or the elderly.
Use blankets or warmers when appropriate.

Flush exposed eyes with plain water or
saline for 15 minutes. Remove contact lenses if easily removable
without additional trauma to the eye. Continue irrigation
during transport to the Critical Care Area.

In cases of ingestion, do not induce
emesis. If the victim is alert and asymptomatic, administer
a slurry of activated charcoal if it has not already been
given (administer at 1 gm/kg, usual adult dose 60-90 g, child
dose 25-50 g). A soda can and straw may be of assistance when
offering charcoal to a child.

Critical Care Area

Be certain that appropriate decontamination
has been carried out (see Decontamination Area above).

ABC Reminders

Patients who are comatose, hypotensive,
or have seizures or cardiac arrhythmias should be treated
in the conventional manner.

Inhalation Exposure

Administer supplemental oxygen by mask
to patients who have respiratory symptoms. Refer to Antidotes
and Other Treatments below for appropriate clinical treatment.

Skin Exposure

Parathion does not generally burn or
irritate the skin, but dermal exposure produces systemic toxicity.
Thorough washing of the skin, as described in Basic Decontamination
above, should be performed and may need to be repeated. Unexplained,
persistent symptoms may indicate inadequate decontamination.

Because of their relatively larger surface
area:body weight ratio, children are more vulnerable to toxicants
affecting the skin.

Eye Exposure

Continue irrigation for at least 15 minutes.
Test visual acuity. Examine the eyes for corneal damage and
treat appropriately. Immediately consult an ophthalmologist
for patients who have severe corneal injuries.

Ingestion Exposure

Do not induce emesis. If the victim
is alert and asymptomatic, administer a slurry of activated
charcoal if it has not already been given (administer at 1
gm/kg, usual adult dose 60-90 g, child dose 25-50 g). A soda
can and straw may be of assistance when offering charcoal
to a child.

Gastric lavage is useful in certain circumstances
to remove toxic material. Consider gastric lavage with a small
nasogastric tube if: (1) a large dose has been ingested; (2)
the patient's condition is evaluated within 30 minutes; (3)
the patient has oral lesions or persistent esophageal discomfort;
and (4) the lavage can be administered within one hour of
ingestion. Care must be taken when placing the gastric tube
because blind gastric-tube placement may further injure the
chemically damaged esophagus or stomach.

Because children do not ingest large
amounts of toxic materials, and because of the risk of perforation
from NG intubation, lavage is discouraged in children unless
performed under endoscopic guidance.

Toxic vomitus or gastric washings should
be isolated, e.g., by attaching the lavage tube to isolated
wall suction or another closed container.

Antidotes and Other Treatments

All patients who have signs or symptoms
of systemic toxicity
require antidotal treatment. In the United States, primary
antidotal treatment for parathion poisoning involves administration
of atropine. In addition, pralidoxime (2-PAM) is indicated
for seriously poisoned patients.

Atropine is a competitive antagonist
of acetylcholine at muscarinic receptors and is used to control
the excessive bronchial secretions which are often responsible
for death. Pralidoxime relieves both the nicotinic and muscarine
effects of organophosphate poisoning by regenerating acetylcholinesterase
and can reduce both the bronchial secretions and the muscle
weakness associated with poisoning.

The initial intravenous dose of atropine
in adults should be determined by the severity of symptoms:
An initial adult dose of 1.0 to 2.0 mg or pediatric dose of
0.01 mg/kg (minimum 0.01 mg) should be administered intravenously.
If intravenous access cannot be established, atropine may
also be given subcutaneously or via endotracheal tube. Doses
should be repeated every 15 minutes until excessive secretions
and sweating have been controlled. Once bronchial secretion
has been controlled, atropine administration should be repeated
whenever the secretions begin to recur. In seriously poisoned
patients, very large doses may be required. Alterations of
pulse rate and pupillary size should not be used as indicators
of treatment adequacy.

Pralidoxime should be administered as
early in poisoning as possible as its efficacy may diminish
when given more than 24 to 36 hours after exposure. Doses
are as follows: adult 1.0 g; pediatric 25 to 50 mg/kg. The
drug should be administered intravenously over 30 to 60 minutes,
but in a life-threatening situation, one-half of the total
dose can be given per minute for a total administration time
of 2 minutes. Treatment should begin to take effect within
40 minutes with a reduction in symptoms and the amount of
atropine necessary to control bronchial secretion. The initial
dose can be repeated in 1 hour and then every 8 to 12 hours
until the patient is clinically well and no longer requires
atropine.

Patients who have seizures most often
respond to atropine and pralidoxime; however, if they do not
respond, administer diazepam or lorazepam.

Avoid other acetylcholinesterase inhibitors
(e.g., physostigmine and edrophonium chloride), and do not
use succinylcholine for rapid sequence intubation. The
paralyzing effects of succinylcholine are likely to be prolonged
because it will not be metabolized normally.

Non-depolarizing neuromuscular blockers
(e.g., pancuronium and vecuronium) may not be effective because
of unsuccessful competition with acetylcholinesterase for
the motor end-plate receptors.

Laboratory Tests

The diagnosis of acute parathion toxicity
is primarily clinical and is based on the combination of nausea,
excessive sweating and salivation, miosis, and muscle weakness.
Routine laboratory studies for all exposed patients include
CBC, glucose, and electrolyte determinations. A chest radiograph
is useful to examine for hydrocarbon aspiration and non-cardiogenic
pulmonary edema. Symptomatic and asymptomatic patients suspected
of significant exposure should have determinations of plasma
and red blood cell (RBC) cholinesterase activity. Symptoms
of acute poisoning are usually present when more than 50%
of RBC cholinesterase activity is inhibited. However, these
tests are not always readily available and are more useful
in diagnosis and follow-up. Blood and urine analyses for the
presence of parathion or its metabolite may show whether damage
has been done to the brain, heart, lungs, and nerves.

Disposition and Follow-up

Patients with life threatening illness
must be hospitalized, also consider hospitalizing patients
who have a suspected serious exposure and are symptomatic.

Delayed Effects

Skin absorption can cause delayed or
recurrent symptoms. Contaminated clothing and leather items
(e.g., shoes, wallets, and belts) should not be reused, even
if they have been washed.

Aspiration of commercial parathion preparations
that contain hydrocarbon solvents can result in chemical pneumonitis.

Chronic neurologic symptoms have been
reported for some patients exposed to organophosphates. Symptoms
develop after acute toxicity has resolved (24 to 96 hours
after exposure) and can include cognitive impairment, depression,
Guillian-Barré syndrome, and peripheral neuropathy.

Patient Release

Patients who remain asymptomatic for
4 to 6 hours after exposure may be discharged with instructions
to seek medical care promptly if symptoms develop (see Parathion-Patient
Information Sheet below).

Follow-up

Obtain the name of the patient's primary
care physician so that the hospital can send a copy of the
ED visit to the patient's doctor.

Patients who have severe exposure should
be evaluated for persistent CNS sequelae and delayed peripheral
neuropathy.

Patients who have been acutely poisoned
should be advised to avoid further organophosphate exposure
until sequential RBC cholinesterase levels have stabilized
in the normal range, a process that may take 3 to 4 months
after severe poisoning.

Patients who have corneal injuries or
severe skin burns should be reexamined within 24 hours.

Reporting

If a work-related incident has occurred,
you may be legally required to file a report; contact your
state or local health department.

Other persons may still be at risk in
the setting where this incident occurred. If the incident
occurred in the workplace, discussing it with company personnel
may prevent future incidents. If a public health risk exists,
notify your state or local health department or other responsible
public agency. When appropriate, inform patients that they
may request an evaluation of their workplace from OSHA or
NIOSH. See Appendices III and IV for a list of agencies that
may be of assistance.

Patient Information Sheet

This handout provides information and
follow-up instructions for persons who have been exposed to
parathion.

Print this handout only. 19k

What is parathion?

Parathion is a potent organophosphate
pesticide. It is a pale yellow-to-brown liquid with an odor
like garlic. It is used by farmers as a pesticide on fruits,
vegetables, nuts, and grains. Commercial pesticides often
contain a hydrocarbon solvent, which itself can cause illness.

What immediate health effects can result from parathion exposure?

Parathion can cause nausea, vomiting,
stomach cramps, and diarrhea, as well as confusion, blurred
vision, sweating, muscle twitching, irregular heartbeat, convulsions,
and death. Symptoms occur when parathion is inhaled, swallowed
or absorbed through the skin. Breathing the solvent used to
dissolve the pesticide may cause dizziness, headache, and
nausea. Generally, the more serious the exposure, the more
severe the symptoms.

Can parathion poisoning be treated?

For minor exposures (for example, breathing
the pesticide solvent), the only treatment needed is fresh
air. For serious parathion poisoning, thorough washing of
all exposed skin, removal and burning of exposed clothing,
and hospitalization and administration of an antidote may
be needed.

Are any future health effects likely to occur?

A single small exposure from which a
person recovers quickly is not likely to cause delayed or
long-term effects. After a serious exposure, a patient may
feel ill for several weeks.

What tests can be done if a person has been exposed to parathion?

Specific tests for the presence of parathion
or its breakdown product in blood and urine generally are
not useful to the doctor. If a severe exposure has occurred,
blood and urine analyses and other tests may show whether
damage has been done to the brain, heart, lungs, and nerves.
Testing is not needed in every case.

Where can more information about parathion be found?

More information about parathion can
be obtained from your regional poison control center; your
state, county, or local health department; the Agency for
Toxic Substances and Disease Registry (ATSDR); your doctor;
or a clinic in your area that specializes in occupational
and environmental health. If the exposure happened at work,
you may wish to discuss it with your employer, the Occupational
Safety and Health Administration (OSHA), or the National Institute
for Occupational Safety and Health (NIOSH). Ask the person
who gave you this form for help in locating these telephone
numbers.

ATSDR can also tell you the location of occupational and environmental health clinics. These clinics specialize in
recognizing, evaluating, and treating illnesses resulting from exposure to hazardous substances.